Advertisement

Zeitschrift für Neurologie

, Volume 198, Issue 1, pp 33–45 | Cite as

The effect of ischemia on sensorimotor cortex of cat

Electrophysiological, biochemical and electronmicroscopical observations
  • K. -A. Hossmann
  • K. Sato
Original Investigations

Summary

Complete cerebral ischemia was produced in normothermic cats by clamping the innominate and subclavian arteries and simultaneous lowering of the systemic blood pressure. The effect of ischemia on the sensorimotor cortex was assessed by neurophysiological, electronmicroscopical, and biochemical observations. Nerve cell excitability, synaptic transmission and EEG activity recovered after ischemia of up to 1 hr. The neurophysiological recovery was paralleled by the restoration of the energy-producing metabolism which approached normal values when spontaneous EEG activity reappeared. Electronmicroscopy revealed the structural preservation of the cortex after the recovery of function.

Keywords

Public Health Blood Pressure Electronmicroscopy Ischemia Cerebral Ischemia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

Literature

  1. Ames III, A., Wright, R. L., Kowada, M., Thurston, J., Majno, G.: Cerebral ischemia. II. The no-reflow phenomenon. Amer. J. Path. 52, 437–453 (1968).Google Scholar
  2. Cantu, R. C., Ames III, A.: Distribution of vascular lesions caused by cerebral ischemia. Neurology (Minneap.) 19, 128–132 (1969).Google Scholar
  3. — DiGiacinto, G., Dixon, J.: Hypotension: A major factor limiting recovery from cerebral ischemia. J. surg. Res. 9, 525–529 (1969).Google Scholar
  4. Chiang, J., Kowada, M., Ames III, A., Wright, R. L., Majno, G.: Cerebral ischemia. III. Vascular changes. Amer. J. Path. 52, 455–476 (1968).Google Scholar
  5. Crowell, J. W., Sharpe, G. P., Lambright, R. L., Read, W. L.: The mechanisms of death after resuscitation following acute circulatory failure. Surgery 38, 696–702 (1955).Google Scholar
  6. Hager, H., Hirschberger, W., Scholz, W.: Electronmicroscopical changes in brain tissue of Syrian hamster following acute hypoxia. Aerospace Med. 31, 379–387 (1960).Google Scholar
  7. Hills, C. P.: Ultrastructural changes in the capillary bed of the rat cerebral cortex in anoxic-ischemic brain lesions. Amer. J. Path. 44, 531–543 (1964).Google Scholar
  8. Hirsch, H., Breuer, M., Künzel, H. P., Marx, E., Sachweh, D.: Über die Bildung von Thrombozytenaggregaten und die Änderung des Hämatokrits durch komplette Gehirnischämie. Dtsch. Z. Nervenheilk. 186, 58–66 (1964).Google Scholar
  9. — Schneider, M.: Durchblutung und Sauerstoffaufnahme des Gehirns. In: Handbuch der Neurochirurgie, Bd. 1, Teil 2, S. 434–552, H. Olivecrona und W. Tönnis, Eds. Berlin-Heidelberg-New York: Springer 1968.Google Scholar
  10. — Scholl, H., Dickmans, H. A., Eisolt, J., Mann, H., Krankenhagen, B.: Über die corticale Gleichspannung nach Überschreiten der Wiederbelebungszeit des Gehirns. Pflügers Arch. ges. Physiol. 301, 351–357 (1968).Google Scholar
  11. Hohorst, H.-J.: L-(+)-Lactat. Bestimmung mit Lactat-Dehydrogenase und DPN. In: Methoden der enzymatischen Analyse. Herausgeb. H. U. Bergmeyer, S. 266–270. Weinheim (Bergstraße): Verlag Chemie 1962.Google Scholar
  12. Hossmann, K.-A., Olsson, Y.: Suppression and recovery of neuronal function in transient cerebral ischemia. Brain Res. (in press).Google Scholar
  13. — Sato, K.: Recovery of neuronal function after prolonged cerebral ischemia. Science 168, 375–376 (1970).Google Scholar
  14. Karnovsky, M. J.: A formaldehyde-glutaraldehyde fixative of high osmolarity for use in electronmicroscopy. J. Cell Biol. 27, 137 A (1965).Google Scholar
  15. Lamprecht, W., Slein, P.: Creatinphosphat. In: Methoden der enzymatischen Analyse, S. 610–616. Herausgeb. H. U. Bergmeyer. Weinheim (Bergstraße): Verlag Chemie 1962.Google Scholar
  16. Langfitt, T. W., Weinstein, J. D., Kassell, N. F.: Cerebral vasomotor paralysis produced by intracranial hypertension. Neurology (Minneap.) 15, 622–641 (1965).Google Scholar
  17. Merker, G.: Ultrastrukturveränderungen motorischer Vorderhornzellen des Kaninchens unter abgestufter Ischämie. Z. Zellforsch. 95, 568–593 (1969).Google Scholar
  18. Müller, U., Hinzen, D. H., Sobotka, P., Gebert, E., Lang, R., Hirsch, H.: Energiestoffwechsel und evozierte Potentiale der Hirnrinde nach kompletter Ischämie in Normothermie. Pflügers Arch. 316, R 77–78 (1970).Google Scholar
  19. Oberdörster, G., Saum, R., Benner, K. U., Gebert, E., Sobotka, P., Hirsch, H.: Die Erholung des Elektrocorticogramms nach kompletter Ischämie des Hundegehirns in Normothermie. Pflügers Arch. 307, R 116–117 (1969).Google Scholar
  20. Slein, M. W.: D-Glucose. Bestimmung mit Hexokinase und Glucose-6-Phosphat-Dehydrogenase. In: Methoden der enzymatischen Analyse, S. 117–123. Herausgeb. H. U. Bergmeyer. Weinheim (Bergstraße): Verlag Chemie 1962.Google Scholar
  21. Webster, H. de F., Ames III, A.: Reversible and irreversible changes in the fine structure of nervous tissue during oxygen and glucose deprivation. J. Cell. Biol. 26, 885–910 (1965).Google Scholar
  22. Yashon, D., White, R. J., Taslitz, N., Wolin, L. R., Massopust, Jr. L. C.: Experimental cerebral circulatory arrest: Effect on electrocortical potentials. J. Neurosurg. 32, 74–82 (1970).Google Scholar

Copyright information

© Springer-Verlag 1970

Authors and Affiliations

  • K. -A. Hossmann
    • 1
  • K. Sato
    • 1
  1. 1.Abteilung für Allgemeine NeurologieMax-Planck-Institut für HirnforschungKöln

Personalised recommendations